Y编码样睾丸特异性蛋白5在心肌缺血再灌注损伤中的保护作用  

The protective role of TSPYL5 in myocardial ischemia/reperfusion injury

作　　者：范怡伦 吴佳伟 丁丹 黄一航 薛松[1] 黄日太[1] FAN Yilun;WU Jiawei;DING Dan;HUANG Yihang;XUE Song;HUANG Ritai(Department of Cardiovascular Surgery,Renji Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200127,China)

机构地区：[1]上海交通大学医学院附属仁济医院心血管外科,200127

出　　处：《国际心血管病杂志》2022年第5期299-302,共4页International Journal of Cardiovascular Disease

基　　金：上海交大医学院附属仁济医院临床科研创新培育基金计划(PYMDT-008)。

摘　　要：目的:观察过表达Y编码样睾丸特异性蛋白5(TSPYL5)对缺氧/复氧损伤后H9c2细胞的影响。方法:检测TSPYL5在小鼠心肌缺血再灌注及心肌细胞缺氧/复氧损伤后的表达水平。根据表达结果上调TSPYL5,以缺氧/复氧后普通H9c2细胞为对照组,相同模型中过表达TSPYL5的H9c2细胞为实验组,比较2组间凋亡水平的差异。结果:TSPYL5在体内、体外实验中表达水平均显著下降(P<0.001)。与对照组相比,缺氧/复氧模型中过表达组p53的蛋白表达水平显著下调(25.52±0.19对47.39±0.40,P<0.05),caspase-3显著下调(60.57±0.26对108.24±0.56,P<0.05),Bcl-2显著上调(45.65±0.22对28.92±0.01,P<0.05),Tunel染色凋亡阳性率显著下调(P<0.01)。结论:TSPYL 5在心肌缺血再灌注及细胞缺氧/复氧后表达下降;过表达TSPYL5可以减轻细胞在缺氧/复氧后的凋亡水平,从而起保护作用。Objective:To explore the effect of TSPYL5 overexpression on H9c2cells after hypoxia/reoxygenation.Methods:We assessed the expression level of TSPYL5after myocardial ischemia/reperfusion in mice and post hypoxia/reoxygenation in H9c2 cells,respectively.Levels of apoptosis were compared between H9c2 cells with overexpression of TSPYL5 and those without overexpression of TSPYL5 after hypoxia/reoxygenation.Results:The expression level of TSPYL5 was significantly decreased in both in vivo and in vitro experiments(P<0.001).In the hypoxia/reoxygenation model,overexpression of TSPYL5 was associated with lower protein levels of p53(25.52±0.19 vs.47.39±0.40,P<0.05) and caspase-3(60.57±0.26vs.108.24±0.56,P<0.05),while Bcl-2 level was elevated(45.65±0.22 vs.28.92±0.01,P<0.05).Meanwhile,the apoptosis level with positive Tunel staining was significantly reduced(P<0.01).Conclusion:This study suggests that overexpression of TSPYL5 may diminish apoptosis after ischemia/reperfusion and hypoxia/reoxygenation,highlighting a myocardial protective effect.

关 键 词：Y编码样睾丸特异性蛋白5 心肌缺血再灌注损伤 缺氧/复氧损伤 凋亡 P53 

分 类 号：R542.2[医药卫生—心血管疾病]